Bilateral sixth nerve palsy with subdural hematoma: a unique presentation of B12 deficiency.

Vitamin B12 is inextricably associated with the development and maintenance of neuronal functions. It is classically associated with subacute combined degeneration and peripheral neuropathy; however, cranial neuropathy is uncommon. We observed the rarest neurological manifestation of B12 deficiency. A 12 months infant had history of lethargy, irritability, anorexia, paleness, vomiting, and neurodevelopmental delay for 2 months. He also developed inattention and altered sleep pattern. His mother noticed bilateral inward rotation of both eyes. On examination, the infant had bilateral lateral rectus palsy. The infant was found to have anemia (7.7g/dL) and severe B12 deficiency (74pg/mL). On MRI, there was cerebral atrophy, subdural hematoma (SDH) and wide cisternal spaces and sulci. On supplementation with cobalamin, he improved clinically though mild restriction of lateral gaze on the left side persists. Follow up MRI showed significant improvement in cerebral atrophy with resolution of SDH. To date, such clinical presentation of B12 deficiency has never been reported. The authors suggest B12 supplementation for at risk population esp at antenatal stage and lactating mothers in national programs. The treatment of this condition should be initiated early to prevent long term sequelae.

Using the Human Response to Illness Model to assess altered level of consciousness in patients with subdural hematomas.

Head injuries are the leading cause of trauma mortality and account for nearly half of all deaths related to trauma injuries. Patients who present with subdural hematomas are at risk for initial damage to the brain, as well as for subsequent brain damage related to re-bleed, ischemia or cerebral edema. These injuries can be acute or chronic in nature, and may be manifested in the patient as an altered level of consciousness. Skilled nursing assessment of altered level of consciousness leads to early nursing and medical intervention, which, in turn, can improve patient outcomes. In this paper, a critical review of the literature will focus on altered level of consciousness in patients presenting with a subdural hematoma. The Human Response to Illness Model will be utilized as a framework for this review. Accordingly, the physiological, pathophysiological, behavioural, and experiential perspectives of altered level of consciousness will be examined. Thus, a comprehensive understanding of this human response and rationale for evidence-based interventions will be established.

Preventing and treating posttraumatic seizures: the human experience.

Posttraumatic epilepsy presents an ideal target for prevention efforts. Traumatic brain injury (TBI) is common, characteristics that put people at high risk such as penetrating injury or subdural hematoma or provoked seizures are easily identified, and the latency between the injury and the onset of epileptic seizures is frequently short. Several drugs have been tested for their ability to prevent provoked seizures and epilepsy after TBI. We describe the design of those studies and their results. Phenytoin and carbamazepine significantly reduce the incidence of provoked seizures. Phenobarbital and the combination of phenobarbital and phenytoin also look promising for reducing provoked seizures, but small sample sizes in the studies evaluating these drugs do not allow definitive conclusions. None of the drugs studied (phenytoin, phenobarbital, their combination, carbamazepine, valproate, or magnesium) have shown reliable evidence that they prevent, or even suppress, epileptic seizures after TBI. For most of the regimens tested (the phenytoin/phenobarbital combination being the exception), the best estimate of effect is under a 25% reduction in posttraumatic seizures, well less than the 50% reduction most studies were designed to detect. The evaluation of the tested drugs has serious limitations, however, and antiepileptic drugs (AEDs) developed since 1980 and other compounds have barely been tested at all. Better understanding the process of epileptogenesis, testing treatments that demonstrate antiepileptogenic effects in the laboratory, and performing thorough preclinical and phase II evaluations before attempting definitive trials should greatly improve the chance of identifying ways to prevent posttraumatic epilepsy, providing the ultimate cure for this condition.

Dystonia associated with pontomesencephalic lesions.

Secondary dystonia is well known subsequent to lesions of the basal ganglia or the thalamus. There is evidence that brainstem lesions may also be associated with dystonia, but little is known about pathoanatomical correlations. Here, we report on a series of four patients with acquired dystonia following brainstem lesions. There were no basal ganglia or thalamic lesions. Three patients suffered tegmental pontomesencephalic hemorrhage and one patient diffuse axonal injury secondary to severe craniocerebral trauma. Dystonia developed with a delay of 1 to 14 months, at a mean delay of 6 months. The patients' mean age at onset was 33 years (range 4-56 years). All patients presented with hemidystonia combined with cervical dystonia, and two patients had craniofacial dystonia in addition. Three patients had postural or kinetic tremors. Dystonia was persistent in three patients, and improved gradually in one. There was little response to medical treatment. One patient with hemidystonia combined with cervical dystonia improved after thalamotomy. Overall, the phenomenology of secondary dystonia due to pontomesencephalic lesions is similar to that caused by basal ganglia or thalamic lesions. Structures involved include the pontomesencephalic tegmentum and the superior cerebellar peduncles. Such lesions are often associated with fatal outcome. While delayed occurrence of severe brainstem dystonia appears to be rare, it is possible that mild manifestations of dystonia might be ignored or not be emphasized in the presence of other disabling deficits.

Face imagery and its relation to perception and covert recognition in prosopagnosia.

BACKGROUND: Face imagery can access facial memories without the use of perceptual stimuli. Current data on the relation of imagery to the perceptual function and neuroanatomy of prosopagnosic patients are mixed, and little is known about the type of facial information patients can access through imagery. OBJECTIVE: The authors wished to determine 1) which lesions abolished face imagery in prosopagnosia, 2) if deficits in perceiving facial structure were paralleled by similar deficits in imagery, and 3) if covert recognition of faces correlated with the degree of residual imagery for faces. METHODS: The authors tested nine prosopagnosic patients who had been tested previously for perception of facial configuration and covert recognition of famous faces. The authors constructed a battery of 37 questions that asked subjects to imagine the faces of two celebrities and to choose which one had a certain facial property. Half were questions about facial features and half were about overall facial shape. RESULTS: Imagery was abolished only by anterior temporal lesions. Imagery for facial shape but not features was degraded by lesions of the right hemisphere's fusiform face area, which severely impaired perception of facial configuration. Feature imagery was degraded only when there was associated left occipito-temporal damage. Covert recognition was found when either configural perception or imagery was severely damaged, but not when both were abnormal. In patients with impaired configural perception, covert recognition correlated with feature imagery, suggesting that feature-based processing may drive residual covert abilities in these patients. CONCLUSION: Although anterior temporal cortex may be the site of facial memory stores, these data also support hypotheses that perceptual areas like the fusiform face area have parallel contributions to mental imagery. The data on covert recognition are consistent with a view that it is the residue of a partially damaged face-recognition network. Covert recognition may reflect the degree of damage across components of a network rather than mark a specific form of prosopagnosia or a dissociated pathway.

[Impaired recognition of faces: implicit recognition, feeling of familiarity, role of each hemisphere]. / Troubles de la reconnaissance des visages: reconnaissance implicite, sentiment de familiarité, rôle de chaque hémisphère.

We report three observations of patients who suffered from impaired face recognition following cerebral lesions. Two had classical prosopagnosia, resulting from bilateral in one case and right unilateral occipito-temporal in the other. They could not differentiate famous face from unknown ones, and did not feel any familiarity. The third patient has a normal feeling of knowing, could distinguish between familiar and unfamiliar faces, but was unable to evoke any biographical information about the personalities. Prosopagnosic patients demonstrated, in an experimental condition of learning face-name pairs, implicit knowledge. We assume that these capacities were dependent of the activation of networks coding familiar faces in memory. Mental imagery of faces were normal in theses two cases. In addition, stimulation of mental imagery in the first patient improved implicit knowledge in forced choice tasks. These cases throws a light on the respective role of each hemisphere in face recognition. The right hemisphere is advantaged in perceptual analysis, and activates, from the perceived faces, mnestic systems which codes for previously encountered faces. It generates feeling of familiarity, probably by the way of specific systems which differs from, and completes, those allowing identification. The left hemisphere enable access to semantic-biographic knowledge in a conscious, verbal and explicit way.

Hematoma subdural intracraneal bilateral en un paciente con leptospirosis / Bilateral intracranial subdural hematoma in a patient with leptospirosis

Presentamos el caso de un varón de 39 años de edad, que en el curso de una leptospirosis grave, con fracaso renal agudo, edema agudo de pulmón e ictericia importante, comienza con manifestaciones clínicas de afección neurológica (cefalea, disartria y paresia de la extremidad superior derecha). Se evidencian en tomografía computarizada (TC) y resonancia magnética (RM) hematomas subdurales múltiples y bilaterales. Leptospira puede producir una vasculitis difusa con lesión capilar, dando lugar a distintas manifestaciones hemorrágicas, concretamente en el sistema nervioso es una causa conocida de hemorragia subaracnoidea; el hematoma subdural intracraneal representa un hallazgo no descrito en la bibliografía revisada (AU)

Blood degradation products play a role in cerebral ischemia caused by acute subdural hematoma.

The pathogenesis of ischemic brain lesions with traumatic hematoma is multifactorial. It has been suggested that the presence of subdural hematoma in patients with severe head injury is associated with elevated intracranial pressure and higher mortality. In this study we created acute subdural mass in the rats by injecting 250 microliters of autologous blood and silicone oil into the subdural space. The goal of this study was to determine the effect of subdural hematoma versus silicone oil on the adjacent brain parenchyma. Twenty-four hours after the injection, of the hematoma in the subdural space in rats produced an extensive zone of underlying ischemic damage but silicone oil did not. This study has shown that pressure alone caused by silicone oil is insufficient to cause significant neuronal damage or loss.

The effect of the glycine site-specific N-methyl-D-aspartate antagonist ACEA1021 on ischemic brain damage caused by acute subdural hematoma in the rat.

Acute subdural hematoma (SDH) complicates about 20% of severely head-injured patients, and death and severe disability frequently result, yet over half of these patients may have been conscious, at some time after injury, implying secondary mechanisms of brain damage. Drugs that block the "excitotoxic" effects of glutamate at the N-methyl-D-aspartate (NMDA) receptor have generally been effective in reducing ischemic brain damage associated with SDH in animal models, yet these agents all appear to be associated with major behavioral side effects, in conscious patients, at neuroprotective doses. We therefore evaluated the effects of treatment with a novel antagonist for the glycine binding site of the NMDA receptor (ACEA1021) upon ischemic brain damage, in the rat SDH model. ACEA1021 may be free of psychomotor effects, and may thus permit high dose therapy in conscious trauma and stroke patients. SDH was produced by the slow injection of 0.4 mL autologous blood into the subdural space overlying the parietal cortex. brain damage was assessed histologically at 8 coronal planes, in animals sacrificed 4 h after induction of hematoma. Both pre- and posttreatment with ACEA1021 significantly reduced hemispheric ischemic damage produced by SDH. The magnitude of neuroprotection with this compound (26 to 39% reduction in infarct size) is similar to other NMDA antagonists, and the robust posttreatment effect implies that human studies with this compound should be performed in head injured patients, subject to completion of toxicology testing.

Managing hypersexual disorders in brain-injured clients.

Three case studies involving hypersexuality in brain-injured clients are illustrated. Two cases involved the inappropriate touching of the opposite sex, and the third case involved exhibitionism. In one case of touching, feedback was used to decrease inappropriate touching. In the other case of touching, scheduled massage was used to shift stimulus control to an appropriate setting. In the case of exhibitionism, a combination of self-monitoring, private self-stimulation and dating-skills training were used to suppress the behaviour.

Alterations in gastric mucosal microvascular endothelium in a stressed condition--relevance to gastric ulcerogenesis.

The present paper describes the morphological and functional alterations of the gastric mucosal microvascular endothelium under restraint-stressed condition. On the basis of the direct cholinergic innervation of capillaries and non-muscular venules in the gastric mucosa, these endothelial changes would be caused by the stress-induced overstimulation of the cholinergic nerves and modified by the degranulation of mast cells, contributing to the stress-induced ulcer formation as schematically illustrated in Fig. 10.